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Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2

Anje Cauwels UGent, Ben Janssen, Anouk Waeytens UGent, Claude Cuvelier and Peter Brouckaert UGent (2003) NATURE IMMUNOLOGY. 4(4). p.387-393
abstract
Dysregulated apoptotic cell death contributes to many pathological conditions, including sepsis, prompting the suggestion that caspase inhibition to block apoptosis could have useful therapeutic applications. Because the cytokine tumor necrosis factor (TNF, also known as TNF-alpha) is both proapoptotic and pro-inflammatory and is involved in septic shock, we tested whether caspase inhibition would alleviate TNF-induced toxicity in vivo. General caspase inhibition by the protease inhibitor zVAD-fmk exacerbated TNF toxicity by enhancing oxidative stress and mitochondrial damage, resulting in hyperacute hemodynamic collapse, kidney failure and death. Thus, survival of TNF toxicity depends on caspase-dependent processes. Our results demonstrated the pathophysiological relevance of caspase-independent, ROS-mediated pathways in response to lethal TNF-induced shock in mice. In addition, survival of TNF toxicity seemed to require a caspase-dependent protective feedback on excessive reactive oxygen species (ROS) formation and phospholipase A2 activation.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
ACTIVATION, MICE, CELL APOPTOSIS, TNF-ALPHA, FAS, SIGNAL-TRANSDUCTION, DEATH DOMAIN, INDUCED ENTEROCYTE APOPTOSIS, DOMAIN KINASE RIP, ARACHIDONIC-ACID RELEASE
journal title
NATURE IMMUNOLOGY
Nat. Immunol.
volume
4
issue
4
pages
387 - 393
Web of Science type
Article
Web of Science id
000181987700020
JCR category
IMMUNOLOGY
JCR impact factor
28.18 (2003)
JCR rank
2/112 (2003)
JCR quartile
1 (2003)
ISSN
1529-2908
DOI
10.1038/ni914
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1087229
handle
http://hdl.handle.net/1854/LU-1087229
date created
2010-12-14 15:29:43
date last changed
2016-12-19 15:44:14
@article{1087229,
  abstract     = {Dysregulated apoptotic cell death contributes to many pathological conditions, including sepsis, prompting the suggestion that caspase inhibition to block apoptosis could have useful therapeutic applications. Because the cytokine tumor necrosis factor (TNF, also known as TNF-alpha) is both proapoptotic and pro-inflammatory and is involved in septic shock, we tested whether caspase inhibition would alleviate TNF-induced toxicity in vivo. General caspase inhibition by the protease inhibitor zVAD-fmk exacerbated TNF toxicity by enhancing oxidative stress and mitochondrial damage, resulting in hyperacute hemodynamic collapse, kidney failure and death. Thus, survival of TNF toxicity depends on caspase-dependent processes. Our results demonstrated the pathophysiological relevance of caspase-independent, ROS-mediated pathways in response to lethal TNF-induced shock in mice. In addition, survival of TNF toxicity seemed to require a caspase-dependent protective feedback on excessive reactive oxygen species (ROS) formation and phospholipase A2 activation.},
  author       = {Cauwels, Anje and Janssen, Ben and Waeytens, Anouk and Cuvelier, Claude and Brouckaert, Peter},
  issn         = {1529-2908},
  journal      = {NATURE IMMUNOLOGY},
  keyword      = {ACTIVATION,MICE,CELL APOPTOSIS,TNF-ALPHA,FAS,SIGNAL-TRANSDUCTION,DEATH DOMAIN,INDUCED ENTEROCYTE APOPTOSIS,DOMAIN KINASE RIP,ARACHIDONIC-ACID RELEASE},
  language     = {eng},
  number       = {4},
  pages        = {387--393},
  title        = {Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2},
  url          = {http://dx.doi.org/10.1038/ni914},
  volume       = {4},
  year         = {2003},
}

Chicago
Cauwels, Anje, Ben Janssen, Anouk Waeytens, Claude Cuvelier, and Peter Brouckaert. 2003. “Caspase Inhibition Causes Hyperacute Tumor Necrosis Factor-induced Shock via Oxidative Stress and Phospholipase A2.” Nature Immunology 4 (4): 387–393.
APA
Cauwels, A., Janssen, B., Waeytens, A., Cuvelier, C., & Brouckaert, P. (2003). Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2. NATURE IMMUNOLOGY, 4(4), 387–393.
Vancouver
1.
Cauwels A, Janssen B, Waeytens A, Cuvelier C, Brouckaert P. Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2. NATURE IMMUNOLOGY. 2003;4(4):387–93.
MLA
Cauwels, Anje, Ben Janssen, Anouk Waeytens, et al. “Caspase Inhibition Causes Hyperacute Tumor Necrosis Factor-induced Shock via Oxidative Stress and Phospholipase A2.” NATURE IMMUNOLOGY 4.4 (2003): 387–393. Print.